1. Kidney-cortex slices incubated with pyruvate formed glucose and lactate in relatively large and approximately equimolar quantities. The formation of these products involves two exclusively cytoplasmic NADH(2)-requiring reductions, catalysed by lactate dehydrogenase and triose phosphate dehydrogenase. From the rates of glucose and lactate formation it can be calculated that over 1000mu-moles of NADH(2) must have been produced in the cytoplasm/g. dry wt. of tissue/hr. 2. When lactate is a gluconeogenic precursor the required NADH(2) is generated in the cytoplasm, but, when a substrate more highly oxidized than glucose, such as pyruvate, is the precursor, there is no direct cytoplasmic source of NADH(2). Quantitative data on the fate of pyruvate are in accord with the conclusion that the NADH(2) was primarily formed intramitochondrially by the dehydrogenases of cell respiration, with pyruvate as the major substrate. 3. Similar observations and conclusions apply to experiments with mouse-liver slices incubated with pyruvate, serine or aspartate. 4. Addition of ethanol, which increases the formation of NADH(2) in the cytoplasm, increased the formation from pyruvate of lactate but not of glucose. 5. In view of the low permeability of mitochondria for NAD and NADH(2) it must be postulated that special carrier mechanisms transfer the reducing equivalents of intramitochondrially generated NADH(2) to the cytoplasm. Reasons are given in support of the assumption that the malate-oxaloacetate system acts as the carrier. 6. Various aspects of the generation of reducing power and its transfer from mitochondria to cytoplasm are discussed.

1. The rate of gluconeogenesis from amino acids and other known precursors in slices of mouse liver after depletion of liver glycogen by means of phlorrhizin was high with l-lactate, pyruvate, glycerol, d-glyceraldehyde, dihydroxyacetone, d-fructose, sorbitol, xylitol, alpha-glycerophosphate, alanine, proline, threonine, serine and propionate. 2. The rate was unexpectedly low or even negligible with glutamate, aspartate, other glucogenic amino acids and the intermediates of the tricarboxylic acid cycle. 3. Glutamine and asparagine gave higher rates than the corresponding amino acids but still much lower rates than kidney cortex. 4. Livers of male mice gave much lower rates than livers of female mice. Kidney cortex showed no sex difference. 5. Livers of mice fed on a low-carbohydrate diet gave the same rates as livers of mice fed on a normal diet under the test conditions, i.e. 3hr. after an injection of phlorrhizin. 6. Much carbohydrate was formed from endogenous precursors and this was accompanied by release of ammonia and urea. 7. Gluconeogenesis in well-fed mice not treated with phlorrhizin was low. 8. Maximum rates were observed 3hr. after phlorrhizin treatment. 9. Prolonged phlorrhizin treatment did not prevent extensive deposition of liver glycogen, after an initial depletion. 10. Gluconeogenesis in livers of mice fed on a high-fat diet was relatively low. 11. Livers of alloxan-diabetic mice had a high carbohydrate content after phlorrhizin treatment, and gluconeogenesis from endogenous sources was about twice as high as in normal animals. Added substrates had about the same effect in normal and diabetic livers.

In a previous publication (Getz & Bartley, 1961) the fatty acid compositions of various intracellular compartments of the rat liver were investigated. This work has now been extended to the fatty acid composition of the different lipid classes of the liver. The data obtained will be used as a basis for comparison of the lipid composition of each of the cell components. This paper reports a compositional analysis of the whole rat liver. EXPERIMENTAL Fractionation of lipids on 8ilicic acid. The techniques of

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